A nuclear lncRNA Linc00839 as a Myc target to promote breast cancer chemoresistance via PI3K/AKT signaling pathway
0301 basic medicine
0303 health sciences
Gene Expression Profiling
Genes, myc
Breast Neoplasms
Original Articles
Xenograft Model Antitumor Assays
3. Good health
Gene Expression Regulation, Neoplastic
Disease Models, Animal
Mice
Phosphatidylinositol 3-Kinases
03 medical and health sciences
Drug Resistance, Neoplasm
Cell Line, Tumor
Animals
Humans
Female
RNA Interference
RNA, Long Noncoding
Proto-Oncogene Proteins c-akt
In Situ Hybridization, Fluorescence
Cell Proliferation
Signal Transduction
DOI:
10.1111/cas.14555
Publication Date:
2020-07-03T15:38:19Z
AUTHORS (9)
ABSTRACT
Abstract Chemoresistance has become a leading cause of mortality in breast cancer patients and is one the major obstacles for improving clinical outcome. Long noncoding RNAs play important roles tumorigenesis chemoresistance. However, involvement regulation lncRNAs chemoresistance are not completely understood. Here, we reported that Linc00839 was localized nucleus upregulated chemoresistant cells tissues, high level associated with poor prognosis. Knockdown significantly suppressed proliferation, invasion, migration, sensitized to paclitaxel vitro inhibited transplant tumor development vivo. Mechanistically, found Myc could directly bind promoter region activate its transcription. Furthermore, overexpression increased expression RNA‐binding protein Lin28B activated PI3K/AKT signaling pathway. We also discovered positively interacted tissues. Taken together, first time, showed by promoted proliferation through binding Lin28B. These findings provide new insight into regulatory mechanism propose Myc/Linc00839/Lin28B feedback loop be used as novel therapeutic target cancer.
SUPPLEMENTAL MATERIAL
Coming soon ....
REFERENCES (44)
CITATIONS (44)
EXTERNAL LINKS
PlumX Metrics
RECOMMENDATIONS
FAIR ASSESSMENT
Coming soon ....
JUPYTER LAB
Coming soon ....